关于miR-335-5p靶向调控MAPK10的表达促进结直肠癌进展的初步探讨

Preliminary Exploration of miR-335-5p Targeting MAPK10 to Promote the Progression of Colorectal Cancer

摘要: 目的：探究丝裂原活化蛋白激酶10 (mitogen-activated protein kinase 10, MAPK10)和miR-335-5p在结直肠癌(colorectal cancer, CRC)中的表达及其两者之间的靶向结合关系。方法：本研究通过TCGA数据库分析CRC与正常结直肠组织中MAPK10和miR-335-5p的转录水平表达差异，并在SW480和Caco2细胞系中提取RNA进行逆转录定量聚合酶链反应。此外，采用双荧光素酶实验验证miR-335-5p与MAPK10的靶向结合关系。结果：TCGA数据分析显示，CRC组织中MAPK10显著低表达(P < 0.05)，miR-335-5p显著高表达(P < 0.001)，且二者表达呈负相关(R = −0.246, P < 0.001)。细胞系实验验证了MAPK10低表达和miR-335-5p高表达的现象。双荧光素酶实验显示miR-335-5p与MAPK10的3'非翻译区存在显著结合(P < 0.05)。结论：miR-335-5p通过与MAPK10的3'UTR结合抑制其表达，提示其在CRC中的潜在调控作用。

Abstract: Objective: To investigate the expression of mitogen-activated protein kinase 10 (MAPK10) and miR-335-5p in colorectal cancer (CRC) and their targeted binding relationship. Methods: In this study, the transcriptional level expression differences of MAPK10 and miR-335-5p between CRC and normal colorectal tissues were analyzed through the TCGA database. RNA was extracted from SW480 and Caco2 cell lines for reverse transcription quantitative polymerase chain reaction (RT-qPCR). Additionally, a dual-luciferase reporter assay was employed to verify the targeted binding relationship between miR-335-5p and MAPK10. Results: TCGA data analysis revealed that MAPK10 was significantly downregulated in CRC tissues (P < 0.05), while miR-335-5p was significantly upregulated (P < 0.001), and their expressions were negatively correlated (R = −0.246, P < 0.001). Cell line experiments confirmed the phenomena of low MAPK10 expression and high miR-335-5p expression. The dual-luciferase reporter assay demonstrated significant binding between miR-335-5p and the 3'untranslated region (3'UTR) of MAPK10 (P < 0.05). Conclusion: miR-335-5p inhibits the expression of MAPK10 by binding to its 3'UTR, suggesting its potential regulatory role in CRC.